Comment on Lee et al. Sodium–Glucose Cotransporter 2 Inhibitors and Risk of Retinal Vein Occlusion Among Patients With Type 2 Diabetes: A Propensity Score–Matched Cohort Study. Diabetes Care 2021;44:2419–2426

We read with great interest the article by Lee et al. (1) showing an increased risk of retinal vein occlusion (RVO) among patients with diabetes initiating sodium–glucose cotransporter 2 inhibitors (SGLT2i) based on a very large Korean cohort.

Beyond this quantitative overview on the risk of RVO across hypoglycemic medications in real life, we would like to highlight one striking point. The additional cases of RVO following SGLT2i initiation (16 supplemental events among the 47,369 patients treated with SGLT2i, i.e., an added risk of 0.034% in 2.5 years) seem to be strongly associated with chronic kidney disease (CKD). Indeed, as shown in Fig. 2 of Lee et al. (1), patients with an estimated glomerular filtration rate (eGFR) of <60 mL/min/1.73 m2 at baseline had a threefold higher RVO risk after initiating SGLT2i, while those with an eGFR of ≥60 mL/min/1.73 m2 had a similar RVO risk regardless of SGLT2i treatment. The additional risk of RVO therefore would be limited to patients with CKD. To better quantify the relationship between RVO risk and CKD, we would be very interested to know the respective number of patients in the CKD population who presented with RVO according to SGLT2i treatment. Additional data regarding the RVO risk in SGLT2i-treated patients with CKD compared with those without CKD would also be informative. It should be noted that a close association between CKD and RVO has been reported in recent studies. A meta-analysis reported that nearly 10% of patients with RVO have CKD and, conversely, patients with end-stage renal disease compared with those without renal failure had a more than twofold increased risk of developing RVO (2). Therefore, CKD may play a confounding role in the observed excess risk of RVO (1) and possibly relieves SGLT2i of its full responsibility for RVO onset. To support this hypothesis, it is assumed that most cases of severe polyuria and dehydration occur on treatment initiation (3) with an early and reversible acute drop in eGFR (4) and, hence, may cause or worsen RVO. Consequently, RVO event rate is expected to peak shortly after initiating SGLT2i and then should decrease, suggesting a transient phenomenon. Moreover, comparing whether the time between SGLT2i initiation and RVO occurrence differs in patients with or without CKD would be illustrative.

Overall, we believe that the increased risk of RVO following SGLT2i initiation should not overshadow the well-documented protective benefit of SGLT2i from kidney protection with an approximately 30% reduction in renal events (3). Finally, the large increase in SGLT2i prescriptions since 2018 in elderly patients with CKD (5), a well-known population at high risk of RVO (2), should urge caution without discouraging prescribers from offering this therapeutic class to the growing number of elderly patients with CKD in the next decades.

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